OBJECTIVETo identify the patterns of airway collapse in patients with obstructive sleep apnea hypopnea syndrome(OSAHS) by dexmedetomidine induced sleep endoscopy.

METHODSForty-five obstructive sleep apnea patients diagnosed by polysomnography were given dexmedetomidine intravenously. Once the patient was sedated in dorsal position, the electronic nasopharyngoscope was inserted transnasally and positioned on five levels of the upper airway sequentially (velum, oropharyngeal lateral wall, tongue base, epiglottis and larynx) to observe and document the collapse. Each level should be observed no less than three apneas. The degree of airway narrowing was calculated by using the ImageTool. No obstruction was defined when the degree of airway narrowing <50%, and complete obstruction when ≥ 75%.

RESULTSIn 45 patients with OSAHS, 1 case showed no obstruction on any level, 6 cases demonstrated obstructions on single level only, and 38 cases demonstrated complete obstructions on multilevel, including 17 cases with complete obstructions on two levels, 15 cases complete obstructions on three levels, and 6 cases complete obstructions on four levels. The patterns of collapse found in the trial were: (1) circumferential stricture by velum collapse was found in 43 patients, and 41 cases showed complete obstructions; (2) the side wall of oropharynx all collapsed in a lateral configuration, and 32 cases showed complete obstructions on this level; (3) anteroposterior swallowing tongue base was common, 11 cases showed partial obstructions on level of tongue base, and 10 cases complete; (4) epiglottic collapses occurred in lateral configuration folding as V shape; in anteroposterior configuration, epiglottis met posterior wall of the pharynx due to swallowing tongue base; the server soften epiglottis obstructed the entrance of the larynx, while the mild soften epiglottis and the collapsed side wall of pharynx came into being obstructions in concentric configuration; (5) the arytenoid area and aryepiglottic fold mucosa inwardly covered the glottis when the obstruction occurred in the larynx.

CONCLUSIONSThe patterns of hypopharynx obstructions in OSAHS patients are multifarious. Lateral oropharyngeal wall, epiglottic and tone base collapse play an important role in the obstructions. The laryngeal obstruction can also be observed.

Adult ; Airway Obstruction ; pathology ; Endoscopy ; methods ; Female ; Humans ; Male ; Middle Aged ; Sleep ; drug effects ; Sleep Apnea, Obstructive ; pathology

OBJECTIVE: To compare the value of video laryngoscope in localization diagnosis of upper airway stricture in obstructive sleep apnea-hypopnea syndrome (OSAHS) between awake and drug-induced sleep. METHOD: Ninety-eight patients of OSAHS were examined with video laryngoscope to locate the upper airway stricture under awake and Midazolam-induced sleep. RESULT: The several stricture levels under awake was 58.2% and it was 77.5% under drug induced sleep. CONCLUSION Several stricture levels of upper airway were founded in most of the patients of OSAHS. The upper airway stricture levels was more in the sleep than in the wake.
Adult ; Female ; Humans ; Laryngoscopes ; Male ; Middle Aged ; Sleep ; drug effects ; Sleep Apnea, Obstructive ; diagnosis ; Videotape Recording ; Wakefulness

OBJECTIVETo assess the biological effects of the six-herb mixture Anti-Insomia Formula (AIF) extract using caffeine-induced insomnia Drosophila model and short-sleep mutants.

METHODSCaffeineinduced insomnia wild-type Drosophila and short-sleep mutant flies minisleep (mns) and Hyperkinetic(Y) (Hk(Y)) were used to assess the hypnotic effects of the AIF in vivo. The night time activity, the amount of night time sleep and the number of sleep bouts were determined using Drosophila activity monitoring system. Sleep was defined as any period of uninterrupted behavioral immobility (0 count per minute) lasting > 5 min. Night time sleep was calculated by summing up the sleep time in the dark period. Number of sleep bouts was calculated by counting the number of sleep episodes in the dark period.

RESULTSAIF at the dosage of 50 mg/mL, effectively attenuated caffeine-induced wakefulness (P<0.01) in wild-type Canton-S flies as indicated by the reduction of the sleep bouts, night time activities and increase of the amount of night time sleep. AIF also significantly reduced sleeping time of short-sleep Hk(Y) mutant flies (P<0.01). However, AIF did not produce similar effect in mns mutants.

CONCLUSIONAIF might be able to rescue the abnormal condition caused by mutated modulatory subunit of the tetrameric potassium channel, but not rescuing the abnormal nerve firing caused by Shaker gene mutation. This study provides the scientific evidence to support the use of AIF in Chinese medicine for promoting sleep quality in insomnia.

Animals ; Caffeine ; Chromatography, High Pressure Liquid ; Disease Models, Animal ; Drosophila melanogaster ; drug effects ; physiology ; Hypnotics and Sedatives ; pharmacology ; therapeutic use ; Mutation ; genetics ; Potassium Channels ; genetics ; Sleep ; drug effects ; Sleep Initiation and Maintenance Disorders ; drug therapy ; Wakefulness ; drug effects

OBJECTIVETo review the current evidence that links smoking to obstructive sleep apnea (OSA) and to discuss some potential mechanisms proposed for these links.

DATA SOURCESWe searched PubMed and Medline to identify studies investigating the interaction between smoking and OSA.

STUDY SELECTIONArticles regarding the relationship between smoking and OSA were selected. Studies considered smoking as a confounding factor were excluded.

RESULTSThe association of smoking and OSA has been confirmed in several studies. The effects of smoking on the pathophysiology of OSA may include smoking-induced upper airway inflammation, stimulant effects of nicotine on upper airway muscles, and a "rebound effect" due to nightly short-term nicotine withdrawal, or all of the above. In addition, the coexistence of OSA and smoking may have more widespread implications for cardiovascular dysfunction in patients with OSA. Finally, OSA might be responsible for the addiction to nicotine.

CONCLUSIONSSmoking may act as a risk factor for OSA and join with OSA in a common pathway to increase the risk of systematic injury. OSA, in turn, may be a predisposing factor for smoking. Thus, smoking cessation is recommended when considering treatment for OSA, and treating OSA may be a necessary precondition for successful smoking cessation.

Asthma ; epidemiology ; etiology ; Bronchi ; drug effects ; Humans ; Nicotine ; pharmacology ; Risk Factors ; Sleep ; physiology ; Sleep Apnea, Obstructive ; epidemiology ; etiology ; Smoking ; adverse effects ; Tobacco Use Disorder ; epidemiology ; etiology

This study is to investigate the sedative and hypnotic effects of a novel compound H1208. The sedative activity of H1208 was investigated by recording the spontaneous locomotor activity of mice. The hypnotic property was evaluated by the latency and duration of sleep (loss of righting reflex) in mice and the effect of hypnotics on sleep pattern of electroencephalogram were studied in conscious, freely moving mice with chronically implanted electrodes. The brain monoamine neurotransmitters levels in mice were measured by high performance liquid chromatography-electrochemical detection. The spontaneous locomotor activity was decreased by 56.7% and 80.2% in H1208 (5 and 25 mg x kg(-1), ip) treated mice, respectively. The loss of righting reflex was directly induced in mice after H1208 (60 mg x kg(-1), ip) administration. The non-rapid eye movement sleep increased significantly by 131% and 259%, respectively, within 3 hours after H1208 (30 and 60 mg x kg(-1), ip) administration. However, the rapid eye movement sleep decreased significantly. The contents of DA in the striatum and cortex and 5-HT in the cortex decreased significantly. These results demonstrated that H1208 has potent sedative and hypnotic effects, which may be closely related to the decreased contents of DA and 5-HT in mouse brain.
Animals ; Brain ; drug effects ; physiology ; Dopamine ; metabolism ; Electroencephalography ; Hypnotics and Sedatives ; pharmacology ; Mice ; Motor Activity ; drug effects ; Serotonin ; metabolism ; Sleep ; drug effects

OBJECTIVETo observe the effects of Herba ephedrae, honey-fried Herba ephedrae and Maxingshigan decoction on pentobabital sodium sleep experiment in mice.

METHODSMale Kunming mice were divided into 11 groups, namely normal saline (NS) group, ephedrine group, 3 Herba ephedrae dose (high, medium, and low) groups, 3 honey-fried Herba ephedrae dose group, and 3 Maxingshigan decoction dose groups. The corresponding drugs were administered intragastrically for 6 consecutive days, and 45 min after the final administration, the mice received intraperitoneal injection of pentobabital sodium, and the latent period and continuous sleeping time were recorded.

RESULTSCompared with high- and low-dose Herba ephedrae groups, Maxinshigan decoction containing equivalent Herba ephedrae significantly increased the sleeping time of the mice (P<0.05). In comparison with NS, the decoction at medium and low doses produced no significant changes in the sleeping time, which, however, was significantly shortened in the other 8 groups (P<0.05). Compared with Herba ephedrae, Maxingshigan decoction and honey-fried Herba ephedrae at equivalent doses showed comparable effects on the sleep latency (P>0.05).

CONCLUSIONUnder the condition of this experiment and with pentobabital sodium-induced sleeping time as the index, honey-fried Herba ephedrae shows no obvious effect in reducing the excitement of the central nervous system, while Maxingshigan decoction can significantly lower the excitement level, the effect of which is inversely correlated to the dose administered.

Animals ; Central Nervous System ; drug effects ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; pharmacology ; Ephedra sinica ; chemistry ; Male ; Mice ; Pentobarbital ; pharmacology ; Random Allocation ; Sleep ; drug effects

OBJECTIVETo determine the effects of ginsenosides Rb1(GSRb1) on learning and memory and expression of somatostatin (SS) in the hippocampus and the frontal cortex in rat model of sleep deprivation (SD).

METHODSRats were randomized into groups of SD 2 d, SD 4 d, SD 6 d, and SD 0 d, while each group was sub-divided into GSRb1 group and normal saline (NS) sub-groups. Rats were intraperitoneal administered with 30 mg/(kg*d) of GSRb1 or NS for 7 d, then the learning and memory abilities were examined by measuring average swimming speed and mean escape latency using Morris maze.Expression of somatostatin was detected with immunohistochemical method and image analysis in the hippocampus and the frontal cortex.

RESULTSCompared with SD 0 d rats, SD rats exhibited significant decrease in the average swimming speed and increase in the escape latency (P <0.01). The expression of somatostatin in the hippocampus was decreased significantly in SD 2 d, SD 4 d and SD 6 d rats (P<0.05). However, decrease was only observed in SD 4 d and SD 6 d rats in the frontal cortex (P <0.05). Parallel comparison between NS control and GSRb1 treated rats demonstrated that rats treated with GSRb1 in each subgroup exhibited faster swimming speed and shorter escape latency (P <0.05). Meanwhile, the expression of somatostatin was increased in SD 2 d, SD 4 d and SD 6 d rats in the hippocampus and in SD 4 d and SD 6 d rats in the frontal cortex (P <0.05), respectively.

CONCLUSIONGSRb1 enhances the expression of somatostatin in sleep deprivation rats and subsequently may improve learning and memory abilities of rats.

Animals ; Brain ; metabolism ; Disease Models, Animal ; Ginsenosides ; pharmacology ; Learning ; drug effects ; Male ; Memory ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sleep Deprivation ; metabolism ; Somatostatin ; metabolism

OBJECTIVETo observe the role of NB127914, a CRF R1 receptor antagonist, in the regulation of neonatal sleep/wake cycle.

METHODSRat pups were surgically implanted with electrodes at postnatal day(PN) 13. At PN 14, 6 hours polysomnographic recording data were continuously collected before and after administration of various doses of NBI 27914, atropine and the same amount of saline.

RESULTSCompared with baseline, rapid eye movement (REM) sleep was significantly reduced and was replaced primarily by non-REM (NREM) sleep in all groups treated with NBI, but not with dimethyl sulfoxide/saline. Atropine suppressed REM sleep significantly and increased wakefulness simultaneously.

CONCLUSIONBlockage of corticotropin-releasing factor (CRF) R1 receptors deprives neonatal rat REM sleep.

Aniline Compounds ; pharmacology ; Animals ; Female ; Male ; Polysomnography ; Pyrimidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone ; antagonists & inhibitors ; Sleep, REM ; drug effects ; physiology ; Wakefulness ; drug effects ; physiology

Brain ; physiology ; Child ; Dyssomnias ; drug therapy ; epidemiology ; etiology ; Humans ; Infant ; Sleep ; drug effects ; Vitamin D ; administration & dosage ; analogs & derivatives ; blood ; Vitamin D Deficiency ; complications ; drug therapy ; epidemiology

BACKGROUNDObstructive sleep apnea hypopnea syndrome, characterized by chronic intermittent hypoxia (CIH), is closely correlated with genioglossus dysfunction. CIH has been identified to mediate mitochondrial damage in genioglossus. It has been reported that endoplasmic reticulum stress (ERS) could be induced by mitochondrial dysfunction. This study aimed to investigate the role of ERS in CIH-induced genioglossus injury, as well as the possible intervention effect of adiponectin (Ad) supplement in rats.

METHODSForty-five male Wistar rats were randomly divided into three groups and submitted to room air (group A, n=15) as a control or CIH (groups B and C, n=15, respectively). Throughout the exposure period, intravenous Ad was given in group C; while intravenous normal saline was simultaneously given in groups A and B. After 35-day exposure, genioglossus samples were obtained from the pentobarbital-anaesthetized rats via surgical dissection, following blood sampling. Western blotting was applied to detect expressions of ERS signals and associated apoptotic pathways in genioglossus. Serum adiponectin levels were assessed via enzyme-linked immunosorbent assay (ELISA).

RESULTSSignificant hypoadiponectinemia was revealed in group B only (P < 0.05). Compared to those in groups A and C, expressions of markers involved in ERS, such as glucose regulated protein 78 (GRP78), p-PERK, phosphorylated eukaryotic initiation factor 2a (p-eIF2a), phosphorylated inositol-requiring transmembrane kinase/endoribonuclease 1a (p-IRE1a), spliced X-Box binding protein 1 (XBP1s) and activating transcription factor 6 (ATF6), were significantly enhanced in group B (all P < 0.01); while no significant difference was shown between groups A and C (all P > 0.05). ERSassociated apoptotic pathways were remarkably activated in group B. The involved markers detected as the expression of CCAAT/enhancer binding protein homologous protein (CHOP), B-cell lymphoma/leukemia associatied X protein (BAX) and caspase-12 were significantly elevated (all P < 0.01). Transvenous adiponectin supplement improved the above CIHinduced pathological changes in group C.

CONCLUSIONBeyond hypoadiponectinemia, CIH could enhance ERS and induce activation of ERS-associated apoptotic pathways in genioglossus, which could be significantly improved by adiponectin supplement.

Adiponectin ; administration & dosage ; therapeutic use ; Animals ; Endoplasmic Reticulum Stress ; drug effects ; Hypoxia ; drug therapy ; physiopathology ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Sleep Apnea, Obstructive ; drug therapy